Published online before print March 2, 2009, doi: 10.1161/CIRCULATIONAHA.108.816546
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(Circulation. 2009;119:1370-1377.)
© 2009 American Heart Association, Inc.
Congenital Heart Disease |
Effects of Regional Dysfunction and Late Gadolinium Enhancement on Global Right Ventricular Function and Exercise Capacity in Patients With Repaired Tetralogy of Fallot
From the Department of Cardiology (R.M.W., I.H., A.M.V., A.J.P., T.G.), Children’s Hospital Boston and Department of Pediatrics, Harvard Medical School, Boston, Mass; and the Department of Medicine (R.W.), University of Toronto, Toronto, Ontario, Canada. Dr Wald is currently at the Division of Cardiology, Peter Munk Cardiac Centre, Toronto General Hospital, and Department of Pediatrics, University of Toronto, Toronto, Ontario, Canada.
Correspondence to Tal Geva, MD, Department of Cardiology, Children’s Hospital Boston, 300 Longwood Ave, Boston, MA 02115. E-mail tal.geva{at}cardio.chboston.org
Received October 2, 2007; accepted January 7, 2009.
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Abstract |
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Background— The underlying mechanisms that contribute to global right ventricular (RV) dysfunction in patients with repaired tetralogy of Fallot are incompletely understood. We therefore sought to quantify regional RV abnormalities and to determine the relationship of these to global RV function and exercise capacity.
Methods and Results— Clinical and cardiac magnetic resonance data from 62 consecutive patients with repaired tetralogy of Fallot were analyzed (median age at follow-up 23 years [limits 9 to 67 years]). Using cardiac magnetic resonance data, 3D RV endocardial surface models were reconstructed from segmented contours, and a correspondence between end diastole and end systole was computed with a novel algorithm. Regional RV abnormalities were quantified and expressed as segmental ejection fraction, spatial extent of dyskinetic area, displacement of dyskinetic area, and score of extent of late gadolinium enhancement. Regional abnormalities of function and hyperenhancement were greatest in the RV outflow tract (RVOT). These regional RVOT abnormalities correlated with global RV ejection fraction: RVOT ejection fraction r=0.64, P<0.0001; RVOT dyskinetic area r=–0.51, P<0.0001; RVOT displacement of dyskinetic area r=–0.49, P<0.0001; and RVOT late gadolinium enhancement score r=–0.33, P=0.01. Peak oxygen consumption during exercise correlated best with RVOT ejection fraction (r=0.56, P=0.0002) compared with the remainder of the RV (r=0.35, P=0.03). The only cardiac magnetic resonance variable independently predictive of aerobic capacity was RVOT ejection fraction (P=0.02).
Conclusion— A greater extent of regional abnormalities in the RVOT adversely affects global RV function and exercise capacity after tetralogy of Fallot repair. These regional measures may have important implications for patient management, including RVOT reconstruction, at the time of pulmonary valve replacement.
Key Words: tetralogy of Fallot • heart defects, congenital • magnetic resonance imaging
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Introduction |
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Right ventricular (RV) dysfunction often complicates the clinical course of patients with repaired tetralogy of Fallot (TOF) and is associated with increased morbidity and mortality.1,2 Although the RV is usually capable of initially adapting to the abnormal loading conditions after TOF repair, global RV dysfunction ultimately results from failure of compensatory mechanisms to accommodate the chronic volume and/or pressure loads.3,4 Although the sequence of events leading to ventricular dysfunction has been studied in detail in conditions affecting the left ventricle (LV),5 the pathophysiology of RV dysfunction in late survivors of TOF repair remains incompletely understood. Investigators have long suspected that scar tissue and/or patch material in the RV outflow tract (RVOT) can adversely affect RV mechanics after TOF repair. Using cardiac magnetic resonance (CMR), 2 recent reports have demonstrated an association between late gadolinium enhancement (LGE) in the RV and global systolic dysfunction.6,7 Another study found worse global RV dysfunction in patients with RVOT aneurysms than in those without aneurysms.8 These studies, however, used predominantly qualitative measures of LGE and regional RV wall-motion abnormalities. The degree to which regional abnormalities can affect global RV function and whether these adversely affect exercise capacity, ventricular arrhythmia, and heart failure, independent of global RV dysfunction, remain unknown. The goal of the present study, therefore, was to quantify regional RV abnormalities by CMR and to determine their relationship to global RV function and exercise capacity.
Clinical Prospective p 1377
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Methods |
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Subjects
Patients were included in the study if they fulfilled the following criteria: (1) They had a diagnosis of TOF repair; (2) they had completed a standardized CMR examination protocol at our laboratory between 2002 and 2005; and (3) they had a contemporary clinical evaluation. Patients were excluded if the technical quality of the CMR data was inadequate for quantitative analysis or if they had pulmonary valve replacement before the CMR study. The study was approved by the Scientific Review Committee of the Department of Cardiology and by the Children’s Hospital Boston Committee on Clinical Investigation.
Patient Data
The following information was abstracted from medical records: Date of birth; gender; anatomic diagnoses; date of, age at, and type of each surgical procedure; date of and age at CMR; and date of and age at most recent clinical evaluation. The most recent clinical evaluations were reviewed through March 2008. Results of contemporary cardiopulmonary exercise tests were recorded. Rhythm and conduction abnormalities were identified from a 15-lead ECG, Holter results, and electrophysiology studies. Symptoms of heart failure (New York Heart Association functional class) and cardiovascular interventions were documented.
Cardiac Magnetic Resonance
The details of the CMR protocol used in our laboratory for assessment of patients with repaired TOF have been published.9 Briefly, studies were performed with a commercially available 1.5-Tesla scanner. Ventricular dimensions and function were assessed with an ECG-gated steady state free-precession cine MR pulse sequence during brief periods of breath-holding in the following planes: Ventricular 2-chamber (vertical long-axis), 4-chamber (horizontal long-axis), and short-axis planes (perpendicular to the ventricular long-axis plane based on the previous 4-chamber images), with 12 to 14 equidistant slices completely covering both ventricles. Flow measurements were performed in the proximal main pulmonary artery with a retrospectively gated velocity-encoded cine MR pulse sequence during free breathing.
LGE imaging was performed in the ventricular short- and long-axis planes 10 to 20 minutes after injection of 0.2 mmol/kg gadopentetate dimeglumine (Magnevist, Berlex Laboratories, Wayne, NJ) through a peripheral venous cannula. Imaging was performed with a commercially available inversion recovery–prepared, ECG-triggered, fast gradient–recalled echo pulse sequence.10 Inversion time was optimized for suppression of signal from the RV myocardium, as described by Desai et al.11
A single investigator (R.M.W.) who was blinded to patient clinical outcomes analyzed the CMR data using commercially available software packages (MASS version 4.0 and FLOW version 2.0, Medis, Leiden, the Netherlands). LV and RV end-diastolic (maximal) and end-systolic (minimal) volumes, mass at end diastole, stroke volumes, and ejection fraction (EF) were measured as described by Alfakih et al.12
Quantitative Analysis of Regional RV Function
A validated triangulation algorithm13 was used to reconstruct 3D models of the RV endocardial surfaces at end diastole and end systole for each patient from the aforementioned steady state free-precession short-axis cine images. The impact of long-axis through-plane motion from base to apex was incorporated into the model with the long-axis cine images, as described previously.14 Analyses of regional wall-motion abnormalities and LGE were restricted to the RV free wall. The reconstructed RV free wall comprised an average of 550 triangles with an average triangle size of 
23 mm2.
Analysis of Segmental EF
For segmental analysis, the RV was divided into 3 longitudinal and 3 vertical regions for a total of 9 segments, as described by Klein et al15 (Figure 1). Segmental EFs were calculated for segments 1 through 9 from the reconstructed segmental 3D data sets at end diastole and end systole. To assess the accuracy of the calculated segmental EFs, quantification of global RV EF by use of the sum of the 3D reconstructed segments was compared in each patient by the standard method of EF calculation.
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Analysis of Regional RV Free Wall Displacement
Using custom software developed by 1 of the investigators (I.H.), the magnitude and direction of RV free wall systolic motion were calculated by establishing a correspondence between the surfaces at end diastole and end systole. For each triangle on the end-diastolic surface, a vector was defined along the local normal, and its intersection with the end-systolic surface was found. The length of the vector between the original triangle center and the intersection point determined the displacement of that triangle. The direction and extent of systolic displacement were subsequently analyzed for each triangle in the RV wall. The direction of systolic displacement was considered inward (negative) if motion was toward the center of the LV and outward (positive) if it was away from it. Positive triangular displacement was labeled dyskinesis (Figure 2A).
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Two quantitative measures were derived with this 3D model of RV free wall motion: (1) The area-weighted spatial extent of dyskinesis, defined as the ratio of the dyskinetic area to total RV free wall area, termed dyskinetic area, and (2) the area-weighted magnitude of dyskinesis (in millimeters), defined as the total displacement of all dyskinetic segments indexed to the total RV free wall area (ie, A1xD1+A2xD2+ ... +AnxDn/total RV free wall area, where A is the triangle area, D is the dyskinetic displacement, and n is the number of triangles in the RV free wall), termed displacement of dyskinetic area.
Quantification of LGE
A single investigator (R.M.W.) who was unaware of patient outcome used LGE images of the ventricles in the short- and long-axis planes to manually segment enhanced areas in the RV free wall. The segments of enhanced pixels were represented in the 3D coordinate system on the reconstructed RV endocardial surface and converted to voxels by accounting for the slice thickness of the image (Figure 2B). For each enhanced voxel, a corresponding triangle on the 3D reconstructed surface was found, and the number of enhanced voxels in each triangle was recorded. An enhancement score was derived and was defined as the area-weighted voxel count per triangle (ie, A1xC1+A2xC2+ ... +AnxCn/total RV free wall area, where A is the triangle area, C is the number of enhanced voxels in a triangle, and n is the number of triangles in the RV free wall). The presence of LGE in the interventricular septum and LV free wall was noted.
Outcomes
The primary clinical outcome was defined as peak oxygen consumption measured by exercise test and expressed as an absolute value (mL · kg–1 · min–1) and as percent of predicted for an age- and gender-adjusted normal population. Subnormal exercise capacity was defined as <85% of predicted, as recommended by the American Thoracic Society/American College of Chest Physicians and by Albouaini et al.16,17 Secondary outcomes included sustained ventricular tachycardia (defined as ventricular tachycardia that lasted 
30 seconds or tachyarrhythmia that required cardioversion) and heart failure symptoms (defined as New York Heart Association class II or higher).
Statistical Analysis
Demographic, clinical, and laboratory characteristics were compared for subjects who had impaired exercise tolerance and those who had normal exercise capacity by use of the Wilcoxon rank sum test for continuous variables and Fisher exact test for categorical variables. Continuous variables were correlated with the Spearman correlation coefficient. Multivariable linear regression was used to evaluate independent relationships between measures of regional RV abnormalities and global RV systolic function and independent relationships between CMR variables and exercise capacity (peak oxygen consumption). Statistical data were analyzed with a commercially available software package (SAS version 9.1.3, SAS Institute, Cary, NC).
The authors had full access to and take full responsibility for the integrity of the data. All authors have read and agree to the manuscript as written.
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Results |
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Subjects
Of the 256 patients with repaired TOF who underwent CMR examination in our laboratory during the study period, 62 satisfied the study criteria. Reasons for exclusion were absent or incomplete LGE data set, prior placement of prosthetic pulmonary valve, and image artifacts related to metallic implants. Table 1 summarizes the demographic, clinical, ECG, and exercise characteristics of the study patients. There were no deaths in this cohort. During follow-up, 19 patients underwent pulmonary valve replacement, and 4 patients had an automatic cardiac defibrillator implanted because of sustained ventricular tachycardia. Table 2 summarizes the CMR data for all patients and compares patients with abnormal to those with normal exercise capacity.
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Validation of Regional RV EF Calculation
There was close correlation (r=0.83, P<0.0001) and agreement (mean bias 3.2%, limits of agreement –7.0% to 13.4%) between RV EF calculated from summation of RV surface-reconstructed segmental volumes and the standard method (Figure 3).
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Effect of Regional Dysfunction on Global RV Systolic Function
Regional EF, percent dyskinetic area, displacement of dyskinetic area, and enhancement score in the 9 RV segments are shown in Table 3. The proportions of patients with regional wall-motion abnormalities and LGE in each of the RV free wall segments are shown in Figure 4. There was good agreement between RV free wall dyskinesis and LGE (P=0.002). Except for small, localized areas of LGE in the superior and inferior septal–free wall junctions and at the site of the ventricular septal defect patch, no significant areas of enhancement were seen in the LV. These areas were not included in further analyses.
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Quantitative measures of regional RV free wall dyskinesis (area-weighted spatial extent of dyskinetic area and displacement of dyskinetic area) inversely correlated with global RV systolic function. Specifically, a larger area of RV free wall dyskinesis was associated with a lower global RV EF (r=–0.54, P<0.0001; Figure 5A), and a greater extent of dyskinetic displacement was similarly associated with lower global RV EF (r=–0.46, P<0.0002; Figure 5B). Furthermore, a higher LGE score correlated with a lower global RV EF (r=–0.34, P<0.0001). Multivariable linear regression with adjustment for potential confounders, including ventricular volume, LV function, and pulmonary regurgitation, demonstrated independent contributions of dyskinetic area (P=0.03, regression coefficient –21.3, SE 9.8) and displacement of dyskinetic area (P=0.003, regression coefficient –62.9, SE 20.6) to global RV EF.
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Given that the majority of segmental dyskinesis and LGE was concentrated in segments that correspond to the RVOT (segments 1, 2, and 4; Figure 4), further analyses evaluated relationships between measures of regional dysfunction involving the RVOT, as compared with the remainder of the RV, on global RV systolic function. The following measures of regional abnormalities in the RVOT were moderately correlated with lower global RV function: Spatial extent of dyskinetic area (r=–0.51, P<0.0001), magnitude of dyskinesis (r=–0.49, P<0.0001), and LGE score (r=–0.33, P=0.01). In comparison, correlations between the RV sinus and global RV EF for the aforementioned variables were weaker or absent (dyskinetic area r=–0.39, P=0.002; magnitude of dyskinesis r=–0.38, P=0.003; LGE score r=0.05, P=0.971).
Effects of Regional RV Dysfunction on Exercise Capacity
Peak oxygen consumption on exercise testing was more strongly correlated with RVOT EF (r=0.56, P=0.0002) than the remainder of the RV (r=0.35, P=0.03). Furthermore, patients with subnormal exercise capacity had a greater degree of global and regional RV dysfunction (Table 2). On univariable analysis, subnormal exercise capacity was more closely associated with RVOT EF (P=0.004) than global RV EF (P=0.012). By linear regression analysis with stepwise selection to evaluate independent predictors of exercise capacity (peak oxygen consumption) and with adjustment for CMR parameters of global and regional RV dysfunction, the only significant CMR variable was RVOT EF (P=0.02, regression coefficient 0.29, SE 0.12).
Effects of Regional RV Dysfunction on Ventricular Tachycardia and Heart Failure Symptoms
By univariable analysis, lower RVOT EF was associated with sustained ventricular tachycardia (P=0.045), whereas global RV EF was not (P=0.06). Additionally, sustained ventricular tachycardia was associated with other RV measures, including higher RV end-diastolic (P=0.011) and end-systolic (P=0.014) volumes, higher RV end-diastolic volume z score (P=0.007), and RV stroke volume (P=0.013).
Compared with patients without heart failure symptoms, those in New York Heart Association functional class II or greater had larger RV end-diastolic (P=0.025) and end-systolic (P=0.003) volumes, higher RV end-diastolic volume z score (P=0.008), higher RV mass (P=0.023), lower global RV EF (P=0.01), and a higher LGE score (P=0.036). Among the parameters of regional RV dysfunction, patients in New York Heart Association functional class II or greater had a higher RVOT enhancement score than those without symptoms (P=0.044).
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Discussion |
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The present study used newly developed quantitative methods to analyze the effects of regional RV wall-motion abnormalities and LGE on global RV systolic function and clinical status in patients with repaired TOF. In addition to demonstrating that regional RV abnormalities contribute to RV dysfunction independent of RV size, degree of pulmonary regurgitation, and other confounding factors, we also found that measures of regional dysfunction were associated with decreased exercise capacity, sustained ventricular tachycardia, and symptoms of heart failure.
Previous studies of regional RV wall-motion abnormalities after TOF repair are difficult to compare, because they predominantly relied on qualitative methods to assess wall motion, did not precisely localize the abnormal regions within the RV free wall, did not systematically examine the association between markers of fibrosis (eg, LGE) and regional wall-motion abnormalities, and/or did not investigate the influence of regional RV dysfunction on clinical outcomes. Although the presence of aneurysms in the RVOT after TOF repair has long been recognized on the basis of x-ray ventriculography, echocardiography, CMR, and CT, little has been known about the hemodynamic effects of these aneurysms on global RV function, despite widespread clinical suspicion of an adverse influence.18,19 Indeed, much of the research on this issue has concentrated on the association between RVOT aneurysms and ventricular tachyarrhythmias.20,21 More recently, Davlouros and colleagues8 have shown that patients with an RVOT aneurysm or akinesis detected by CMR had a lower global RV EF. In contrast to the present study, however, the presence of an aneurysm or akinesis was based on visual inspection, was not quantified, and was subject to through-plane motion artifacts.
The importance of fibrosis and/or nonviable tissue such as patch material in the RVOT was highlighted by Oosterhof et al6 and Babu-Narayan et al.7 The present study also found that in addition to the immediate area of the RVOT, LGE frequently extended to the anterior RV free wall and neighboring segments (Figure 4B), and the presence of LGE was associated with regional RV dysfunction. Notably, unlike the findings of Babu-Narayan et al,7 who reported LGE in the LV of 53% of their patients, we did not encounter significant areas of LGE in the LV of patients in the present cohort. This discrepancy is likely related to the frequent use of transapical LV vent during surgery in their patients, as well as to differences in myocardial preservation techniques.7
Clinical Implications
Current management strategies in late survivors of TOF repair aim to restore pulmonary valve competency either by surgical or transcatheter approaches and to control arrhythmias.4,22–25 Several studies have demonstrated either lack of improvement or even decline in RV function, as well as inconsistent electrophysiological responses, after pulmonary valve implantation; however, the reasons for the unpredictable results have not been fully elucidated.25–31 Given the association between RVOT dyskinesis/fibrosis and global RV dysfunction demonstrated in the present study, it is reasonable to speculate that when left untreated, these abnormalities will likely continue to adversely affect RV function and functional capacity. The clinical importance of subnormal exercise tolerance in adults with congenital heart disease is highlighted by the study of Diller et al,32 which evaluated a large cohort composed predominantly of patients with repaired TOF and which showed that decreased peak oxygen consumption on exercise test predicts hospitalization or death. The present data provide evidence that 1 of the possible mechanisms for exercise intolerance late after TOF repair relates to abnormalities of RVOT function.
Although most surgical reports on pulmonary valve replacement describe either limited resection of a localized, discrete aneurysm in the RVOT or no specific measures to address dyskinetic or fibrotic RV wall segments,27–31,33 we found that fibrosis and dyskinesis often extend beyond the superior aspect of the RVOT (the site of pulmonary valve implantation) into adjacent segments (Figures 2 and 4
), which suggests that more extensive remodeling of the RV might be necessary for optimal functional recovery. The clinical benefit of this approach has been demonstrated in patients with LV aneurysms treated by surgical ventricular remodeling.34 Of note, a recent computational modeling study based on in vivo CMR data from patients with repaired TOF has demonstrated that compared with limited RVOT resection, aggressive exclusion of fibrotic/dyskinetic segments in the RV free wall led to reduced local stress/strain conditions and may lead to improved functional recovery of the RV.35 Our institution has an ongoing prospective clinical trial designed to evaluate whether extensive RV remodeling at the time of pulmonary valve replacement leads to improved functional recovery and/or reduced arrhythmia propensity.
Study Limitations
The present study cohort does not represent the entire spectrum of patients with repaired TOF, at least in part because of the exclusion of patients with pacemakers and implantable defibrillators and the selective use of CMR in infants and young children; however, the patient characteristics in the present cohort are similar to those published by other centers.22,33,36 In addition, the study design was predominantly cross-sectional, with a relatively short follow-up interval from CMR to latest clinical evaluation (median 3 years). A more complete realization of the prognostic value of regional RV abnormalities may require longer follow-up. Because exercise data were available in only 38 of 62 patients, there may not have been adequate power to detect differences in CMR variables based on exercise capacity. Similarly, the study might have been underpowered to detect more nuanced associations between measures of regional abnormalities and clinical outcomes, and milder abnormalities such as hypokinesis were not examined. In addition, we performed comparisons on 20 CMR variables, thus increasing the possibility of type I error due to multiple comparisons. Finally, although our software for analysis of regional RV function is not commercially available, the methodology has been validated previously and adds little more than a few minutes of additional processing time to a clinical CMR study.13
Conclusions
A greater extent of regional abnormalities in the RVOT adversely affects global RV function and exercise capacity after TOF repair. These findings support further refinement of treatment strategies designed to address these regional abnormalities, ideally based on a patient-specific approach.
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Acknowledgments |
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Sources of Funding
This work was supported in part by the National Institutes of Health (NIH/NHLBI 1P50 HL074734-01 to Drs Geva, Haber, and Powell).
Disclosures
None.
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Guest Editor for this article was Robyn J. Barst, MD.
Related Article:
Circulation 2009 119: 1353-1354.
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